Anti-Bacterial Defences


  Before a bacterium can infect body tissues, it must first gain entry. There are several non-specific defence mechanisms which help prevent this.

  The skin forms a physical barrier, impermeable to many bacteria. This is further protected by acidic secretions which are toxic to some varieties.

  The epithelial surfaces of the airways and digestive tract are another possible route of entry. They are washed by mucosal secretions, and low pH contributes to the protection of some mucosal surfaces. Throughout the body, non-pathogenic commensal organisms help block establishment of pathogens.

  There are three ways in which bacteria can affect the body adversely. They may invade the tissues and multiply, colonise the tissue surface and cause damage by releasing toxins into the tissues, or thirdly, they may do both; invade and release toxins.

  If these general defences prove inadequate, other more specific mechanisms come into play.

  Take as an example of the first type, N.gonhorroeae in the genito-urinary tract. Normally bacteria are flushed out by the passage of urine.

   In order to attach to the epithelial surface, the bacillus must bind using some receptor. The body's cells attempt to pre-empt this by blocking those receptors.

   Immunoglobulin A is produced by B-cells which may be transported across the epithelium from the abluminal to the luminal surface. To do this, it first becomes bound to the poly-Ig receptor on the abluminal surface of the epithelial cell.

    The cell draws in the IgA bound to its receptor, and forms a vesicle which migrates towards the external, luminal surface.

    At the luminal surface, the IgA is released by cleavage of the receptor and is secreted into the genito-urinary tract.

    When the IgA encounters a bacterium, it can bind to its surface receptors. This prevents the bacterium from attaching to the epithelium, and it is washed away by the passing fluid.

  Another possible route of entry for bacteria is through broken skin, for example C.tetani, the causative agent of tetanus. A bacterial colony could become established following a wound.

   The bacteria multiply and release toxins into the surrounding tissue.

   If the individual has been immunised against tetanus, tetanus specific toxin immunoglobulin exists in tissue serum. When it encounters the bacterial toxins, it binds and blocks the deleterious effect this toxin has on neuronal transmission. The bacterial colony will be phagocytosed in the same way as any bacillus within the body.

    Should the protective effects of IgA be inadequate, and bacteria succeed in attaching to the tissue wall, such as the epithelium in the gut, they will divide on the luminal surface and invade the underlying tissue. An example of this is seen with S.Typhi, the causative agent of typhoid fever.

    The bacteria can invade macrophages and survive within them. However, if there are specific T-cells which recognise bacterial peptides, presented by the macrophage, then the T-cells release interferon gamma which activates the macrophages to destroy the bacteria they have taken up.

    Antibodies and complement in the serum also provide their own immune response to these bacteria, by damaging their membranes and limiting their invasiveness.

    As the immune system has evolved these mechanisms, bacteria have also evolved counter measures to avoid destruction. Some attempt to evade the macrophages by intercepting the chemotactic messengers sent out by the complement system. Without the presence of C3a and C5a, the macrophages cannot determine the site of infection.

   If some bacteria are engulfed by macrophages, they release substances which inhibit the fusing of lysosomes with the vacuole, thus preventing contact with the macrophage's arsenal of chemicals. Those that do allow the lysosome to join with the vacuole can have defences against the reactive species they bring in.

  Others are adapted to survive in the hostile environment of the vacuole through the presence of extremely resistant coatings. Some follow the premise that the best defence is offence. They are able to escape the vacuole into the safety of the cytoplasm of the macrophage, where they divide, and can even kill the host.